The heart may be viewed as a spontaneous current generator whose pumping action is effected by spontaneous generation of an electrical impulse (known as an action potential), conduction of the electrical impulse throughout the heart, and subsequent contraction of the heart muscle (myocardium) in response to the impulse. It is, therefore, electrical activity which initiates and controls muscular contraction of the heart.
Chemicals in the form of ions (such as sodium, potassium and chloride) reside in the extracellular and intracellular fluid of a muscle cell. The concentration gradients of these ions combined with cell membrane features make for a special ion arrangement at the inner and outer wall of the cell membrane. At rest, this special membrane arrangement produces a negative transmembrane potential. If the cell membrane is stimulated by an electrical impulse of adequate magnitude and proper polarity, a process known as an "action potential" will ensue. During an action potential a cell depolarizes (transmembrane potential becomes less negative) and then repolarizes (transmembrane potential returns to resting value). The impulse of adequate magnitude naturally comes from a neighboring cell undergoing an action potential. Thus, impulses are propagated through the heart via a cell-to-cell mechanism.
The heart's electrical impulse originates in the sino-atrial node and is transmitted (cell-to-cell) to all portions of the atria, resulting in the contraction of the atrial chambers. The electrical impulse continues in its path to reach a cluster of conduction fibrils known as the atrioventricular node, or the A-V node. By delaying conduction for approximately one-tenth of a second, the A-V node acts as a buffer for impulses from the atria to the ventricles. This allows for proper flow of blood from the atria to the ventricles.
Following this delay, the A-V node transmits an impulse that reaches another cluster of fibers known as the bundle of His which comprises left and right bundle branches of the His-Purkinjie system. The bundle branches terminate with the Purkinjie fibers which are themselves attached directly to the myocardial cells.
A coordinated wave of electrical impulses effects contraction of many myocardial cells simultaneously, thus causing the heart's pumping action. The action begins in the sino-atrial node from which impulses are provided spontaneously and periodically. The impulses travel to the surrounding cardiac tissue and propagate as a wave of depolarization. As noted above, contracting of the cardiac muscle of the atria follows after the depolarization. Subsequent ventricular conduction is initiated via the A-V node and the His-Purkinjie system.
Normal electrical function provides for continued proper functioning of the heart. However, aberrations in electrical origination or transmission produce concomitant malfunctions of the systemic delivery of blood to the body. The majority of cases of cardiac malfunction may be traced to a failure in the electrical conduction system of the heart. The result of such an electrical failure or change from the normal electrical activity and sequence of cardiac activity is an arrhythmia. Arrhythmias may be atrial, atrioventricular, or ventricular. Two of the most deadly forms of arrhythmia are ventricular tachycardia and ventricular fibrillation. Both of these events are generally defined as sustained ventricular arrhythmias.
In ventricular tachycardia, the sequence of ventricular extrasystoles occur at a rate of between 110 to 240 cycles per minute. This type of arrhythmia is characterized by atrioventricular dissociation, an abnormally wide QRS complex (surface lead electrodes), and a far more rapid rate than usual.
Ventricular fibrillation sometimes preceded by a sustained ventricular tachycardia reaches a frequency in excess of 330 cycles per minute. Ventricular fibrillation is not a cessation of electrical activity, but is actually characterized by incoherent electrical activity throughout the ventricle. This loss of succinct conduction of electrical activity prevents any reasonable contraction of the heart and therefore prevents pumping of blood to the body. If therapy is not given, beyond five minutes inadequate blood will result in loss of brain function and, beyond ten minutes, death will occur.
Several methods are known to treat arrhythmia. Drugs are occasionally prescribed, and, while having significant side effects, are often justified because of the severity of the arrhythmia. Drugs, called calcium antagonists, mediate the heart's conduction by halting electrical conduction through the blocking of the calcium channels of myocardial cells. Nitrates may be used as treatment in cases of acute myocardial infarction or congestive heart failure.
Another therapeutic technique is referred to as radio frequency ablation which is directed to neutralizing accessory electrically-conductive pathways of the heart which cause the heart to fail in properly conducting electrical impulses due to some small area of the heart which is skewing the direction of depolarization. In this technique, a catheter is introduced into the heart and a delivery of high frequency radio waves is used to burn away the faulty area of the heart. Following successful radio frequency ablation therapy, normal conduction of the heart will return and the particular arrhythmia associated with the damaged tissue will be eliminated.
One of the most common approaches for termination of an arrhythmia, instead of prevention, is electrical therapy in which electrodes are fitted to either the body or the heart for selectively delivering an electrical current or shock to alter the rhythm of the heart. Implantable cardioverter defibrillators, or "ICDs", are devices which are implanted and stimulate the heart directly using function generators with specific waveforms to respond to and treat arrhythmias on an "as-needed" basis.
Implantable cardioverter defibrillators have achieved overwhelming success in salvaging thousands of lives by providing immediate electrical therapy for the treatment of potentially lethal arrhythmias, i.e., ventricular tachycardia and ventricular fibrillation. These rhythms are believed responsible for over 80% of cases of sudden cardiac death, which claims 400,000 victims per year. The number of implants of ICDs is exceptional (over 75,000 implants to date), despite its relative infancy in the medical field.
Because of the difference in rates of ventricular extrasystoles between ventricular tachycardia and ventricular fibrillation, a lower amount of defibrillating energy is required for the former than for the latter. An implantable cardioverter defibrillator capable of correctly distinguishing between the two so as to deliver only as much power as the circumstance warrants would produce greater power savings, a situation which is important to extending the life of the unit.
There are known implantable cardioverter defibrillators which supply immediate defibrillation for ventricular fibrillation and lower-energy therapies of antitachycardia pacing and cardioversion for ventricular tachycardias, the object being largely for the conservation of battery power, but also for greater patient comfort. In general, these devices use heart rate to distinguish ventricular tachycardia from ventricular fibrillation.
More particularly, to distinguish between ventricular tachycardia and ventricular fibrillation, commercially available ICDs increment a counter associated with a detection zone based on the most recent cycle length. Measuring cycle length is dependent on an accurate sensing of each depolarization by a trigger. However, electrogram dropout (missed triggers) during ventricular fibrillation produces low estimates of the ventricular fibrillation rate which severely overlap ventricular tachycardia rates making ventricular tachycardia and ventricular fibrillation indistinguishable. (This is particularly problematic in the event of tachyarrhythmias in the range of 200 ms to 350 ms since there is a significant overlap in cycle lengths. See, for example, Caswell et al., Ventricular Tachycardia Discrimination By Antitachycardia Devices, PACE 1996 (unpublished)!.) Such electrogram dropouts are common in ventricular fibrillation because of rapidly changing peak amplitudes.
The implantable cardioverter defibrillators commercially available today use rate thresholds and counters to distinguish ventricular tachycardia and ventricular fibrillation. These methods have had limited success for distinctions between ventricular tachycardia and ventricular fibrillation. Other algorithms have been developed in the research setting with some success.
Compensation for ventricular fibrillation sensing limitations, in order to ensure detection of ventricular fibrillation, is typically achieved by lengthening the fibrillation detection interval (FDI), the rate threshold between ventricular tachycardia and ventricular fibrillation. The overriding necessity of fail-safe ventricular fibrillation detection bypasses the use of lower energy therapies tailored for ventricular tachycardia since overly-liberal FDI values invoke defibrillation for many episodes of ventricular tachycardia. Accordingly, due to the necessity of not missing ventricular fibrillation, physicians program devices to deliver defibrillation to these cases, limiting the usefulness of lower energy therapies which save precious battery energy and decrease patient anxiety.
Little information is available concerning discrimination of ventricular tachycardia from ventricular fibrillation for appropriate therapeutic choice of treatment. Some studies claim defibrillation was delivered to true ventricular fibrillation in only 10-21% of shock episodes. (See, for example, Bardy et al., Implantable Transvenous Cardioverter-Defibrillators, Circulation 1993, 87:1152-1168, and Bardy et al., Clinical Experience With A Tiered-Therapy Multiprogrammable Antiarrhythmia Device, Circulation 1992, 85:1689-1698.) Another study used simulators of the three FDA-approved ICDs to test a variety of ventricular tachycardias and ventricular fibrillations (Caswell et al., Ventricular Tachycardia Discrimination By Antitachycardia Devices, PACE 1996 unpublished!). At nominal parameters, ventricular tachycardia was misdiagnosed as ventricular fibrillation, of greater than 65% of the cases. The PSC invention has been demonstrated to be successful in separating ventricular fibrillation from ventricular tachycardia and sinus rhythm and gives a dramatic improvement over ICD rate methods in current use. Comparatively, one test showed ICDs has specificity of 10% versus 100% specificity for PSC.
In addition to rate, two morphological algorithms for ventricular fibrillation detection were implemented in earlier ICDS, probability density function (PDF) and temporal electrogram analysis (TEA). PDF, the original AICD.TM. detection scheme, used the derivative to define departure from baseline (Mirowski et al., The Automatic Implantable Defibrillator, Am. Heart J. 1980, 100: 1089-1092). TEA, incorporated in some second-generation devices, identified a change in electrogram morphology by the order which depolarizations crossed predetermined thresholds (Paul et al., Temporal Electrogram Analysis: Algorithm Development, PACE 1990, 13: 1943-1947). Experience with PDF and TEA in first- and second-generation devices was disappointing due to its lack of specificity. As a result, by 1992, less than 15% of ICDs utilized either algorithm for tachycardia discrimination (DiCarlo et al., Tachycardia Detection By Antitachycardia Devices: Present Limitations And Future Strategies, Journal of Interventional Cardiology, 1994, 7: 459-472).
A number of studies have begun to address the problem of separating ventricular tachycardia and ventricular fibrillation. In several studies (see, for example, DiCarlo et al., Differentiation Of Ventricular Tachycardia From Ventricular Fibrillation Using Intraventricular Electrogram Morphology, Am. J. Cardiol., 1992, 70: 820-822 and Jenkins et al., Is Waveform Analysis A Viable Consideration For Implantable Devices Given Its Computational Demand?, Computer in Cardiology, 1993, Los Alamitos: IEEE Computer Society Press, 1993: 839-842) the standard deviation of template-based (TB) algorithms (correlation waveform analysis (CWA), bin area method (BAM), difference of area (DOA), derivative area method (DAM)) was used as a discriminant function and achieved varying degrees of success. Sensitivity ranged from 83% to 100% and specificity from 56% to 100%. Other algorithms utilized statistical methods and are discussed in Thakor et al., Ventricular Tachycardia And Fibrillation Detection By A Sequential Hypothesis Testing Algorithm, IEEE Trans. Biomed Eng., 1990, 37:837-843 and Turner et al., Statistical Discriminant Analysis of Arrhythmias Using Intracardiac Electrograms, IEEE Transactions On Biomedical Engineering 1993, 40:985-989. However, neither study segregated the data into training and test sets thus results are inconclusive.
As described by Chen et al. in Ventricular Fibrillation Detection By A Regression Test On The Autocorrelation Function (Medical and Biological Engineering and Computing, 1987, 25: 241-149), autocorrelation function (ACF) was examined using linearity of the peak values where more linearity indicated monomorphic waveforms and achieved 100% sensitivity and specificity.
Two algorithms (discussed and disclosed in Throne et al., Scatter Diagram Analysis: A New Technique For Discriminating Tachyarrhythmias, PACE 1994, 17:1267-1275 and Ropella et al., Differentiation Of Ventricular Tachyarrhythmias, Circulation 1990, 82:2035-2043) using two distinct signals from the ventricle achieved significant success in discriminating ventricular fibrillation from other rhythms. As described in Throne et al., (supra), corresponding pairs of the two channels were plotted on a scatter diagram (SD). It was found that monomorphic ventricular tachycardias trace nearly the same path and occupy a smaller percentage of SD than non-regular rhythms such as polymorphic ventricular tachycardia (PMVT) or ventricular fibrillation. The development of a two channel algorithm using two separate catheters based on the magnitude squared coherence (MSC) which measures the basic organization of the rhythm in the frequency domain was described by Ropella et al. in Differentiation Of Ventricular Tachyarrhythmias (Circulation 1990, 82: 2035-2043). Lastly, U.S. Pat. No. 5,193,535, issued Mar. 16, 1993, to Bardy et al. for METHOD AND APPARATUS FOR DISCRIMINATION OF VENTRICULAR TACHYCARDIA FROM VENTRICULAR FIBRILLATION AND FOR TREATMENT THEREOF describes an algorithm which uses variability of the timing difference (TIM) between two ventricular signals. The method and apparatus of this reference teaches the quantification of the directional changes in the depolarization of the ventricle.
Each of these teachings suffers from at least one disadvantage. Specifically, the described algorithms may be potentially confounded by atrial fibrillation with ventricular response (AF/FVR) due to its variable rate (ACF), and ventricular premature depolarizations (VPDs) due to variable morphology (ACF, TB, TIM, SD). Other possible limitations of these algorithms include computational complexity, the necessity of a sinus rhythm template which is representative of all time and the introduction of multiple electrode catheters.
Accordingly, the present challenge is to optimize differentiation of ventricular tachycardia from ventricular fibrillation in order to direct appropriate therapy to minimize power consumption of an implantable battery-operated device.